How did you arrive at the twin-cycle hypothesis?
The basis of the hypothesis was the work that I had done to try and understand how the body and, in particular, how the liver was controlling the glucose level. I found that the fat in the liver makes it resistant to insulin and glucose production is far too high in type 2 diabetes [patients]. If we reduce the amount of fat in the liver, the insulin sensitivity goes back to normal. That explains the control of sugar in type 2 diabetes. So, this was 2008. And, I put that together with another thought which was if it is too much fat in the liver that is causing this, type 2 diabetes has to be a simple condition. It is always associated with putting on a little bit more weight than ideal. So, I put together my thoughts on the liver with what is happening where the insulin was produced, which is the pancreas. And I said, 'What if it is too much fat in the pancreas that is causing the problem of not making enough insulin? 'Because not only does the insulin not work because of insulin resistance but also not enough insulin is being made rapidly after eating. As I played with these ideas on a piece of paper and drew arrows between the things, I could see it all work as two vicious cycles.
One vicious cycle in the liver would cause a steady buildup of fat in the liver, but then that fat is going to be exported. That is what the liver does. It just gives fat to the rest of the body. If it is too much fat in the liver, maybe too much fat is coming out of it as well and settling in the pancreas and other places. And then that would cause blood sugar to go higher, and that will make more fat in the liver. So we have two vicious cycles, which are interacting.
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